Alzheimer’s disease (AD) is the most common neurodegenerative disorder of the central nervous system. Because disease risk increases with age, the growing expectancy of life will lead to a dramatic increase of cases in Europe and other parts of the world within the next decades. Besides an enormous psychological strain for the affected individuals, the disease will also cause a massive economic damage due to the high degree of disability of the patients. Although the scientific community currently favors a central role of an overproduction of the neurotoxic Aß-peptide in Alzheimers pathogenesis, first studies aiming to attack this pathway revealed disappointing results. The molecular details of pathogenesis still remain unclear.

Exploiting novel mouse models, this Neuronetwork investigates the role of decreased brain levels of the neurotrophic protein BDNF in AD pathogenesis, because a BDNF decline had been observed in patients earlier. Emphasis is laid on the efficiency of memory, which is explored by various learning paradigms. In addition, mitochondrial dysfunction and oxidative stress are analyzed. Following sufficient basic characterization, the disease models offer the possibility to evaluate strategies of neuronal protection, such as physical and mental stimulation, BDNF-substitution, receptor agonists or deep brain stimulation.